Literature Review Neonatal jaundice is benign most of the time, but should be monitored because of the risk of encephalopathy. Known causes include maternal diabetes, prematurity, blood incompatibility, asphyxia and glucose-6-phosphate deydrogenase (G6PD) deficiency. This last one causes haemolysis but it was proposed that hyperbilirubinaemia is not a result of it but rather a decrease in hepatic conjugation, explained by the association with polymorphism of UGT.
Objectives To estimate the role of G6PD deficiency as a risk factor for jaundice in neonates and to estimate the risk of increased morbidity due to this deficiency.
Methods Case–control study, including all neonates who were in phototherapy at NICU/HCPA from March to December in 2007, born with more than 35 weeks of gestational age and weight greater than 2000 g, excluding sepsis, cephalohaematoma, cholestasis. Controls were not jaundiced neonates. Informed consent form was applied. Blood from umbilical cord was collected and enzyme activity was determined by a quantitative method and defect in G6PD was confirmed with PCR. Patients were followed for outcomes as days of phototherapy, need for readmission and neurological sequelae.
Results 494 neonates were admitted, the prevalence of G6PD deficiency was 5% among jaundiced versus 3.3% (not significant). There were no differences between the two groups in the extremes of bilirubin and haemoglobin values, neither about outcomes.
Conclusion Our results showed that routine screening for G6PD deficiency in icteric patients is not indicated in our neonates. The study of the UGT1A1 polymorphism, already observed in other populations, is presently in progress.
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